期刊
FRONTIERS IN PHYSIOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2021.626096
关键词
Nr1d1; exercise; skeletal muscle; atrophy; mitochondrial biogenesis
类别
资金
- Sao Paulo Research Foundation (FAPESP) [2017/09038-1, 2017/12765-2, 2018/12519-4]
- National Council for Scientific and Technological Development (CNPq) [301279/2019-5]
- Coordination for the Improvement of Higher Education Personnel (CAPES) [001]
In the study of acute response to endurance exercise, upregulation of Nr1d1 mRNA levels in oxidative muscle was observed, along with enhanced expression of genes related to mitochondrial biogenesis and atrophy. The investigation also revealed that higher Nr1d1 gene expression in muscle was associated with upregulation of AMPK signaling and mitochondrial-related genes in isogenic mice families.
The nuclear receptor subfamily 1, group D member 1 (Nr1d1), plays a role in the skeletal muscle's oxidative capacity, mitochondrial biogenesis, atrophy genes, and muscle fiber size. In light of the effects of physical exercise, the present study investigates the acute response of Nr1d1 and genes related to atrophy and mitochondrial biogenesis on endurance and resistance exercise protocols. In this investigation, we observed, after one bout of endurance exercise, an upregulation of Nr1d1 in soleus muscle, but not in the gastrocnemius, and some genes related to mitochondrial biogenesis and atrophy were enhanced as well. Also, analysis of muscle transcripts from diverse isogenic BXD mice families revealed that the strains with higher Nr1d1 gene expression displayed upregulation of AMPK signaling and mitochondrial-related genes. In summary, a single session of endurance exercise can enhance the Nr1d1 mRNA levels in an oxidative muscle.
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